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Ohm, thanks for this. What are your thoughts on why there was such a robust anti-LL antibody response in these two monkeys but not in sub-q LL trials (that I remember)?

Could this explain the less than stellar therapeutic response in the 700mg LL arm of the MASH/NASH trial along with sample size and possible single allele delta 32 deletions in some of the patients?

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The antibody response might be as simple as a slow ramp up of the production of leronlimab in the AAV version giving the body time to mount a heavy antibody response. With subcutaneous leronlimab the very fast rate of receptor occupation would mean a diminished response. The high level of antibodies may also be partially due to genetic variation causing an overactive immune response.

Since the MASH trial was all subcutaneous, genetic variation outside of single allele may be a small contributing factor but probably not related to anything else in the AAV study.